Of interest to us is the link between increased circulating levels of nutrients and overactive mTOR in T cells.
This overactive state leads to inhibition of the expression of regulatory T cells, also known as Tregs,which are important suppressor agents of autoimmunity.
By inhibiting TOR, rapamycin can prevent autoimmunity by increasing the activity of Tregs.
"Systemic lupus erythematosus (SLE) patients exhibit T-cell dysfunction which can be regulated through the mitochondrial transmembrane potential (Δψm) and mammalian target of rapamycin (mTOR) by glutathione. Therefore, the safety, tolerance, and efficacy of glutathione-precursor N-acetylcysteine (NAC) were examined in this randomized double-blind placebo-controlled study…
…NAC increased Δψm (p=0.0001) in all T cells, it profoundly reduced mTOR activity (p=0.0001), enhanced apoptosis (p=0.0004) and reversed expansion of CD4−/CD8− T cells (1.35 ± 0.12-fold; p=0.008), stimulated Foxp3 expression in CD4+/CD25+ T cells (p=0.045), and reduced anti-DNA production (p=0.049)."
I think the role of rapamycin in expanding the Treg population of T cells is very important in regulating autoimmunity. I’m very impressed by several studies suggesting a role for rapamycin in both preventing and treating MS since it may help to replete the myelin sheath.
One note of concern is that TOR2 is involved in the production of autoantibodies, but we’re concerned about inhibiting it to any significant degree. It’s all very complicated.